Researchers are studying mechanisms of human infection by animal viruses. The investigators induce random mutations in the genome of an avian influenza virus that is unable to infect humans but is structurally similar to human influenza A virus. A mutated isolate is found to be able to infect human upper respiratory tract epithelial cells. Alteration in which of the following viral components most likely enabled this novel strain to cause cross-species infection?

Question

Researchers are studying mechanisms of human infection by animal viruses.  The investigators induce random mutations in the genome of an avian influenza virus that is unable to infect humans but is structurally similar to human influenza A virus.  A mutated isolate is found to be able to infect human upper respiratory tract epithelial cells.  Alteration in which of the following viral components most likely enabled this novel strain to cause cross-species infection?

Quizplus · Accepted Answer

Influenza virus is a segmented, negative-sense RNA virus that is enveloped within a host-derived plasma membrane. Interaction with the host cell is dependent upon a viral surface glycoprotein called hemagglutinin, which binds to the sialic acid receptor on human respiratory epithelial cells. Influenza strains that are unable to infect humans (eg, avian/swine influenza) encode for hemagglutinin that cannot bind to human cells. However, influenza is prone to antigenic changes in its surface glycoproteins due to: Antigenic changes to hemagglutinin can alter the tissue tropism of the virus and allow strains that previously only affected livestock (eg, avian, swine) to infect human cells. (Choice B) The influenza lipid bilayer envelope is generated from host cells during viral replication. Because it is composed of host cell lipids, it is unlikely to be significantly altered by viral mutations. (Choices C, D, and E) Following influenza attachment and endocytosis, the viral bilayer envelope fuses with the endosome membrane, which liberates the nucleocapsid protein (bound to the RNA genome), viral RNA-dependent RNA polymerase, and viral mRNA endonuclease into the cytoplasm. These travel to the nucleus to initiate viral replication. Although mutations to these proteins could affect viral replication, they would be unlikely to alter tissue tropism because they are not on the surface of the virus and, therefore, do not mediate viral attachment. Educational objective: The tissue tropism of viruses is primarily mediated by viral surface glycoproteins that bind to specific host cell receptors. Mutations to viral surface glycoproteins can alter tissue tropism and cause noninfective viruses to become infectious.

Researchers Are Studying Mechanisms of Human Infection by Animal Viruses